Indeed, inhibition of brain AChEis a well-established mechanism of action of anti-AD drugs, with threeout of the four currently marketed drugs being AChE inhibitors.26 Strikingly, the increased levels of ACh thatresult from AChE inhibition may promote arachidonic acid metabolismto EETs, upon activation of ACh muscarinic M1 receptors,27 thereby potentiating the anti-neuroinflammatoryeffects of EETs. The gene discussed is ACHE; the disease is Alzheimer disease.